The axons of the retinal ganglion cells pass through the cribiform plate of the eye to form the optic nerve. Changes in pressure across the cribiform plate cause the cribiform plate to bow. As a consequence of the altered shape of the cribiform plate, optic nerve fibers are damaged and this results in glaucoma which is relatively common and is manifested by cupping of the optic nerve head, visual field defects, and blindness.
Cribiform Plate
The opening in the posterior sclera, where the retinal ganglion axons exit the eye to form the optic nerve, is called the optic nerve canal. The cribiform plate is a mesh like structure extending across the optic nerve canal and is formed from the collagen and elastic fibers of the inner two thirds of the sclera. The retinal ganglion axons pass through the cribiform plate to form the optic nerve. Generally, the cribiform plate is bowed out from the eye. With increased intraocular pressure bowing of the cribiform plate increases, causing damage to the axons as they pass through the mesh of the cribiform plate. Any increase in the differential pressure across the cribiform plate will alter the shape of the cribiform plate, which can cause damage to optic nerve fibers; i.e., glaucomatous optic neuropathy.
Optic Nerve Head
The optic nerve head is formed by retinal ganglion axons as they exit the eye through the cribiform plate to form the optic nerve. Generally the retinal ganglion axons are unmyelinated and only become myelinated once they pass through the cribiform plate to form the optic nerve fibers. There are approximately 1.2 million retinal ganglion axons. The retinal ganglion axons from the macular area run almost horizontally to the optic nerve head, while those from the surrounding areas follow an arcuate pattern. The center of the optic nerve head contains the central retinal arteries and veins. The central edge of the retinal ganglion axons in the optic nerve head that surround the central arteries and veins forms the optic nerve cup. As a consequence of increased intraocular pressure, or a reduction of the perfusion pressure of the capillary supply to the optic nerve fibers, the cribiform plate bows casing damage to the optic nerve fibers at and distal to the cribiform plate. Importantly, damage to the optic nerve fibers distal to the cribiform plate occurs before any damage to the retinal ganaglion axons. With time, the retinal ganglion axons proximal to the cribiform plate eventually die causing the optic cup to enlarge, generally more vertically than horizontally, and the central blood vessels shift toward the outer edge of the optic nerve head. This enlargement of the cup of the optic nerve head is sine qua non for glaucoma. Opthalmoloscopy and fundus photography are generally used to assess the size of the optic nerve cup.
Visual Field
The visual field is defined as the extent of the physical space visible with each eye. The average visual field of each eye, when viewing straight ahead, is approximately 95° temporally, 60° nasally, 65° superiorly and 60° inferiorly. All normal eyes have a blind spot in the temporal visual field. The nasal edge of the blind spot is located approximately 15° temporal to the point of central fixation. The normal blind spot is oval with its major axis extending vertically for approximately 7° and it minor axis extending horizontally for approximately 5°. The center of the blind spot is located approximately 1.5° below the horizontal line of sight. The blind spot is the visual representation of the optic nerve head. Enlargement of the blind spot may be an early sign of retinal ganglion axonal death.
Perimetry
Perimeters are used to measure the extent of a patient's visual field. Perimeters generally use the location of the blind spot to insure proper fixation. Present perimeters rely on the subjective response of the patient's detection of a flashing light, or a moving target or a flickering sinusoidal grating to measure the visual field. The target can be different sizes and/or different colors. The light intensity and/or color of either the background and/or the target is altered to subjectively measure the threshold of the response in different areas of the visual field. There are manual perimeters, which require the operator to record the patient's response, and there are automatic perimeters, which automatically record the patient's response. The automatic perimeters have sophisticated computer algorithms to reduce the time of recording the patient' response and to improve the accuracy of the record. However, all perimeters have the disadvantage of depending on the subjective response of the patient.
Glaucoma Detection
One of the major uses of the perimeter is to detect glaucoma. Glaucoma generally occurs as a consequence of elevated intraocular pressure. The increase in intraocular pressure causes retinal ganglion axonal death in a unique pattern, which is manifested by an enlargement of the cup of the optic nerve and a visual filed defect consisting of an arcuate scotoma. The arcuate scotoma corresponds to the arcuate pattern of the damaged retinal ganglion axons. With continued elevated intraocular pressure, more of the retinal ganglion cells die and the visual field becomes reduced to just a small central area which eventually is lost and the patient becomes completely blind. Early detection of retinal ganglion axonal loss is paramount to preventing visual loss and blindness. It has been demonstrated that cupping of the optic nerve occurs before the manifestation of visual field defects. Measurements of the thickness of the retinal ganglion axon layer at and near the optic nerve further demonstrate that retinal ganglion axons may be destroyed before perimetric evidence of their death.
Measurement of Retinal Ganglion Axonal Death
There are numerous methods for detecting retinal ganglion axonal death. These methods either involve measuring the relationship of the size of the cup of the optic nerve to the size of the head of the optic nerve, and/or the thickness of the retinal ganglion axonal layer at or near the optic nerve head. These measuring methods include fundus photography, polarimetry, and optical coherent tomography. The disadvantage of these methods is they can only detect loss of retinal cell axons; i.e., after they have died.
Glaucoma Prevention and Treatment
In order to prevent the deleterious effects of glaucomatous optic neuropathy, intraocular pressure is lowered either medically and or surgically; however, even with therapy many patients go blind.
Consequently, there is a need in the art for a device that can prevent glaucomatous optic neuropathy.